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Introduction
Schizophrenic patients have an increased lifetime risk of co-morbid obsessive-compulsive symptoms (OCS). These are characterized by obsessive, distressing, intrusive thoughts and related compulsions (Poyurovsky et al. 2004). Epidemiological studies reported that about 30% of schizophrenics meet diagnostic criteria of obsessive-compulsive disorder (OCD) (Buckley et al. 2009; Mukhopadhaya et al. 2009). Conversely, only 1.7% of OCD patients suffer from co-morbid psychotic symptoms (de Haan et al. 2009). Co-morbid OCD is associated with pronounced positive and negative symptoms and lower levels of social functioning and rehabilitation (Lysaker et al. 2004; Öngür & Goff, 2005; Cunill et al. 2009; Guillem et al. 2009). The neurobiological pathogenesis is not clearly understood. The co-morbid sample comprises heterogeneous subgroups, most probably distributed on a dimensional spectrum between typical OCD and schizophrenia. OCD patients without insight might represent a subgroup with genetic, phenotypic and therapeutic vicinity to the schizophrenia-like spectrum (Tumkaya et al. 2009; Catapano et al. 2010). Further concepts propose 'schizotypic OCD' (Poyurovsky & Koran, 2005; Poyurovsky et al. 2008) or 'schizo-obsessive schizophrenia' (Hwang et al. 2000; Bottas et al. 2005; Reznik et al. 2005; Sevincok et al. 2006; Rajkumar et al. 2008). However, a subgroup of co-morbid patients experiences OCS manifestation only after the onset of antipsychotic treatment. Starting with the observations of De Haan et al. (1999), followed up by Lykouras et al. (2003), several studies suggested OCS induction by antiserotonergic second-generation antipsychotics (SGAs) (de Haan et al. 2004; Reznik et al. 2004; Kwon et al. 2009). SGAs significantly differ in their pharmacodynamic properties, in particular regarding inherent serotonergic blockade, monoaminergic reuptake inhibition or even partial serotonergic agonism (Shapiro et al. 2003; Meltzer & Huang, 2008; Meltzer & Sumiyoshi, 2008; Remington, 2008; Lopez-Gil et al. 2010). While predominantly dopaminergic SGAs such as amisulpride (Scatton et al. 1997) or the partial dopaminergic/serotonergic agonist aripiprazole (Sparshatt et al. 2010) appear to be beneficial or at least neutral regarding OCS (Connor et al. 2005; Zink et al. 2006; Englisch & Zink, 2008; Kim et al. 2008; Englisch et al. 2009), clozapine (Coward, 1992; Meltzer, 1994) and olanzapine (Bymaster et al. 1997) seem to bear an inherent risk of OCS induction most probably due to their antiserotonergic properties (Reznik et al. 2004; Öngür & Goff,...